The steroid hormone ecdysone directs Drosophila metamorphosis via thre
e heterodimeric receptors that differ according to which of three ecdy
sone receptor isoforms encoded by the EcR gene (EcR-A, EcR-B1, or EcR-
B2) is activated by the orphan nuclear receptor USP. We have identifie
d and molecularly mapped two classes of EcR mutations: those specific
to EcR-B1 that uncouple metamorphosis, and embryonic-lethal mutations
that map to common sequences encoding the DNA-and ligand-binding domai
ns. In the larval salivary gland, loss of EcR-B1 results in loss of ac
tivation of ecdysone-induced genes. Comparable transgenic expression o
f EcR-B1, EcR-B2, and EcR-A in these mutant glands results, respective
ly, in full, partial, and no repair of that loss.